Placenta mediates the association between maternal second-hand smoke exposure during pregnancy and small for gestational age

Niu, Zhongzheng; Xie, Chuanbo; Wen, Xiaozhong; Tian, Fei; Ding, Peng; He, Yuan; Lin, Jianmiao; Yuan, Shuguang; Guo, Xiaoli; Jia, Deqin; Chen, W.-Q.

doi:10.1016/j.placenta.2015.05.005

Cited by 24 publications

(10 citation statements)

References 30 publications

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“…There are multiple factors which contribute to PBIs such as placental insufficiency, inflammation, infection, toxicity, and genetics. This study focuses on PBI caused by placental insufficiency (PI) [4]. The placenta is a vital organ in fetal development as it is responsible for transporting nutrients and oxygen to the fetus from the mother [4].…”

Section: Introductionmentioning

confidence: 99%

“…This study focuses on PBI caused by placental insufficiency (PI) [4]. The placenta is a vital organ in fetal development as it is responsible for transporting nutrients and oxygen to the fetus from the mother [4]. PI manifests as an inadequate transfer of oxygen and nutrients to the fetus by a reduced supply of blood; this results in a hypoxic-ischemic (HI) environment for the fetus [5,6].…”

Section: Introductionmentioning

confidence: 99%

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Sulforaphane (SFA) protects neuronal cells from oxygen & glucose deprivation (OGD)

et al. 2021

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Background Perinatal brain injury results in neurodevelopmental disabilities (neuroDDs) that include cerebral palsy, autism, attention deficit disorder, epilepsy, learning disabilities and others. Commonly, injury occurs when placental circulation, that is responsible for transporting nutrients and oxygen to the fetus, is compromised. Placental insufficiency (PI) is a reduced supply of blood and oxygen to the fetus and results in a hypoxic-ischemic (HI) environment. A significant HI state in-utero leads to perinatal compromise, characterized by fetal growth restriction and brain injury. Given that over 80% of perinatal brain injuries that result in neuroDDs occur during gestation, prior to birth, preventive approaches are needed to reduce or eliminate the potential for injury and subsequent neuroDDs. Sulforaphane (SFA) derived from cruciferous vegetables such as broccoli sprouts (BrSps) is a phase-II enzyme inducer that acts via cytoplasmic Nrf2 to enhance the production of anti-oxidants in the brain through the glutathione pathway. We have previously shown a profound in vivo neuro-protective effect of BrSps/SFA as a dietary supplement in pregnant rat models of both PI and fetal inflammation. Strong evidence also points to a role for SFA as treatment for various cancers. Paradoxically, then SFA has the ability to enhance cell survival, and with conditions of cancer, enhance cell death. Given our findings of the benefit of SFA/Broccoli Sprouts as a dietary supplement during pregnancy, with improvement to the fetus, it is important to determine the beneficial and toxic dosing range of SFA. We therefore explored, in vitro, the dosing range of SFA for neuronal and glial protection and toxicity in normal and oxygen/glucose deprived (OGD) cell cultures. Methods OGD simulates, in vitro, the condition experienced by the fetal brain due to PI. We developed a cell culture model of primary cortical neuronal, astrocyte and combined brain cell co-cultures from newborn rodent brains. The cultures were exposed to an OGD environment for various durations of time to determine the LD50 (duration of OGD required for 50% cell death). Using the LD50 as the time point, we evaluated the efficacy of varying doses of SFA for neuroprotective and neurotoxicity effects. Control cultures were exposed to normal media without OGD, and cytotoxicity of varying doses of SFA was also evaluated. Immunofluorescence (IF) and Western blot analysis of cell specific markers were used for culture characterization, and quantification of LD50. Efficacy and toxicity effect of SFA was assessed by IF/high content microscopy and by AlamarBlue viability assay, respectively. Results We determined the LD50 to be 2 hours for neurons, 8 hours for astrocytes, and 10 hours for co-cultures. The protective effect of SFA was noticeable at 2.5 μM and 5 μM for neurons, although it was not significant. There was a significant protective effect of SFA at 2.5 μM (p<0.05) for astrocytes and co-cultures. Significant toxicity ranges were also confirmed in OGD cultures as ≥ 100 μM (p<0.05) for astrocytes, ≥ 50 μM (p<0.01) for co-cultures, but not toxic in neurons; and toxic in control cultures as ≥ 100 μM (p<0.01) for neurons, and ≥ 50 μM (p<0.01) for astrocytes and co-cultures. One Way ANOVA and Dunnett’s Multiple Comparison Test were used for statistical analysis. Conclusions Our results indicate that cell death shows a trend to reduction in neuronal and astrocyte cultures, and is significantly reduced in co-cultures treated with low doses of SFA exposed to OGD. Doses of SFA that were 10 times higher were toxic, not only under conditions of OGD, but in normal control cultures as well. The findings suggest that: 1. SFA shows promise as a preventative agent for fetal ischemic brain injury, and 2. Because the fetus is a rapidly growing organism with profound cell multiplication, dosing parameters must be established to insure safety within efficacious ranges. This study will influence the development of innovative therapies for the prevention of childhood neuroDD.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Sulforaphane (SFA) protects neuronal cells from oxygen & glucose deprivation (OGD)

et al. 2021

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“…Al respecto existen fuertes evidencias sobre la asociación entre el tabaquismo materno durante el embarazo y la restricción del crecimiento intrauterino [44][45][46], sin embargo, los efectos de esta exposición sobre el crecimiento lineal postnatal no están bien definidos [47]. Se ha señalado que debido a la disminución de la vascularización de la placenta y por tanto del área de intercambio de gases y nutrientes entre la madre y el feto, se origina un retardo en el crecimiento intrauterino [48] además de malnutrición fetal, condicionando a los lactantes a IMC bajos durante su desarrollo. Adicional a esto, se ha reportado que los componentes del humo del tabaco limitan la absorción y utilización del complejo vitamínico B, disminuyen los niveles de ácido fólico, vitaminas A y C en niños, lo cual favorece el estrés oxidativo e influye en su estado nutricional [49].…”

Section: Discussionunclassified

Función renal, niveles urinarios de cadmio y plomo en niños del municipio de Naguanagua (estado Carabobo, Venezuela), expuestos a humo de tabaco ambiental

Medina

Figueredo

et al. 2018

archmed

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Objetivo: los metales presentes en las fases gaseosa y particulada del humo del tabaco ambiental, son considerados nefrotóxicos. En esta investigación se evaluó la función renal y niveles urinarios de cadmio y plomo en niños expuestos al humo de tabaco ambiental en una comunidad del municipio Naguanagua (Carabobo, Venezuela). Materiales y métodos: la muestra estuvo conformada por 43 niños (21 expuestos y 22 no expuestos), a quienes se les determinó en orina puntual índices urinarios cadmio/creatinina, plomo/creatinina, albúmina/creatinina, calcio/creatinina, fosfatasa alcalina/creatinina y β-2-microglobulina/creatinina. Resultados: en el grupo expuesto existe una correlación positiva y significativa entre β-2-microglobulina/creatinina y albúmina/creatinina independientemente del género y la edad. Los valores absolutos de los marcadores nefrotóxicos correlacionaron positiva y significativamente con sus índices, lo que indica que es útil la corrección con creatinina, con excepción de la Fosfatasa Alcalina la cual refleja mejor su utilidad diagnóstica en valores absolutos. Plomo/creatinina, β-2-microglobulina y Calcio/creatinina mostraron diferencias estadísticamente significativas al estratificar la muestra según grupo etario. La excreción urinaria de cadmio, tanto el grupo expuesto como el control supera ciertos puntos de corte descritos en investigaciones internacionales. Conclusiones: la evaluación de la toxicidad renal debe contar con el monitoreo de varios marcadores, dado que algunos serán más sensibles a los cambios precoces debido a exposiciones crónicas.

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“…A review by Clifton and Murphy [80] has stated that disregarding the sex of the fetus whilst studying the placenta is improper practice. While some studies do follow this advice [81, 82], most studies disregard the sex of the fetus and pool placental samples (e.g. [17–19, 23]).…”

Section: Limitations In Placental Transport Studiesmentioning

confidence: 99%

Placental transporter localization and expression in the Human: the importance of species, sex, and gestational age differences†

Walker

Filis

Soffientini

et al. 2017

Biology of Reproduction

107

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The placenta is a critical organ during pregnancy, essential for the provision of an optimal intrauterine environment, with fetal survival, growth, and development relying on correct placental function. It must allow nutritional compounds and relevant hormones to pass into the fetal bloodstream and metabolic waste products to be cleared. It also acts as a semipermeable barrier to potentially harmful chemicals, both endogenous and exogenous. Transporter proteins allow for bidirectional transport and are found in the syncytiotrophoblast of the placenta and endothelium of fetal capillaries. The major transporter families in the human placenta are ATP-binding cassette (ABC) and solute carrier (SLC), and insufficiency of these transporters may lead to deleterious effects on the fetus. Transporter expression levels are gestation-dependent and this is of considerable clinical interest as levels of drug resistance may be altered from one trimester to the next. This highlights the importance of these transporters in mediating correct and timely transplacental passage of essential compounds but also for efflux of potentially toxic drugs and xenobiotics. We review the current literature on placental molecular transporters with respect to their localization and ontogeny, the influence of fetal sex, and the relevance of animal models. We conclude that a paucity of information exists, and further studies are required to unlock the enigma of this dynamic organ. Summary SentenceThis review summarises the existing knowledge of human placental molecular transporters (SLC and ABC superfamilies). We highlight areas where greater and more accurate knowledge is required and discuss weaknesses of animal models for the human.

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Placenta mediates the association between maternal second-hand smoke exposure during pregnancy and small for gestational age

Cited by 24 publications

References 30 publications

Sulforaphane (SFA) protects neuronal cells from oxygen & glucose deprivation (OGD)

Sulforaphane (SFA) protects neuronal cells from oxygen & glucose deprivation (OGD)

Función renal, niveles urinarios de cadmio y plomo en niños del municipio de Naguanagua (estado Carabobo, Venezuela), expuestos a humo de tabaco ambiental

Placental transporter localization and expression in the Human: the importance of species, sex, and gestational age differences†

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